| Autor: |
Salas-Perez F; Health Sciences Institute, Universidad de O'Higgins, Rancagua 2820000, Chile., Assmann TS; Graduate Program in Medical Sciences, Endocrinology, Department of Internal Medicine, Faculty of Medicine, Federal University of do Rio Grande do Sul, Porto Alegre 90035-003, Brazil., Ramos-Lopez O; Medicine and Psychology School, Autonomous University of Baja California, Tijuana 22390, Mexico., Martínez JA; Center for Nutrition Research, University of Navarra, 31008 Pamplona, Spain.; Department of Nutrition, Food Science and Physiology, University of Navarra, 31008 Pamplona, Spain.; Centro de Investigación Biomédica en Red de la Fisiopatología de la Obesidad y la Nutrición (CIBERobn), Carlos III Health Institute, 28029 Madrid, Spain., Riezu-Boj JI; Center for Nutrition Research, University of Navarra, 31008 Pamplona, Spain.; Navarra Institute for Health Research (IdiSNA), 31008 Pamplona, Spain., Milagro FI; Center for Nutrition Research, University of Navarra, 31008 Pamplona, Spain.; Department of Nutrition, Food Science and Physiology, University of Navarra, 31008 Pamplona, Spain.; Centro de Investigación Biomédica en Red de la Fisiopatología de la Obesidad y la Nutrición (CIBERobn), Carlos III Health Institute, 28029 Madrid, Spain.; Navarra Institute for Health Research (IdiSNA), 31008 Pamplona, Spain. |
| Abstrakt: |
Changes in gut microbiota composition and in epigenetic mechanisms have been proposed to play important roles in energy homeostasis, and the onset and development of obesity. However, the crosstalk between epigenetic markers and the gut microbiome in obesity remains unclear. The main objective of this study was to establish a link between the gut microbiota and DNA methylation patterns in subjects with obesity by identifying differentially methylated DNA regions (DMRs) that could be potentially regulated by the gut microbiota. DNA methylation and bacterial DNA sequencing analysis were performed on 342 subjects with a BMI between 18 and 40 kg/m 2 . DNA methylation analyses identified a total of 2648 DMRs associated with BMI, while ten bacterial genera were associated with BMI. Interestingly, only the abundance of Ruminococcus was associated with one BMI-related DMR, which is located between the MACROD2 / SEL1L2 genes. The Ruminococcus abundance negatively correlated with BMI, while the hypermethylated DMR was associated with reduced MACROD2 protein levels in serum. Additionally, the mediation test showed that 19% of the effect of Ruminococcus abundance on BMI is mediated by the methylation of the MACROD2 / SEL1L2 DMR. These findings support the hypothesis that a crosstalk between gut microbiota and epigenetic markers may be contributing to obesity development. |
